Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.
Science Careers Booklet

Site Tools

  • AAAS
  • Subscribe
  • Feedback

Site Search

Search Advanced

Originally published in Science Express on 28 February 2008
Science 21 March 2008:
Vol. 319. no. 5870, pp. 1683 - 1687
DOI: 10.1126/science.1152864
Prev | Table of Contents | Next

Reports

Protein Synthesis and Neurotrophin-Dependent Structural Plasticity of Single Dendritic Spines

Jun-ichi Tanaka,1,2,3* Yoshihiro Horiike,1,2* Masanori Matsuzaki,1,2,3,4 Takashi Miyazaki,1,2,3 Graham C. R. Ellis-Davies,5 Haruo Kasai1,2,3{dagger}

Long-term potentiation (LTP) at glutamatergic synapses is considered to underlie learning and memory and is associated with the enlargement of dendritic spines. Because the consolidation of memory and LTP require protein synthesis, it is important to clarify how protein synthesis affects spine enlargement. In rat brain slices, the repetitive pairing of postsynaptic spikes and two-photon uncaging of glutamate at single spines (a spike-timing protocol) produced both immediate and gradual phases of spine enlargement in CA1 pyramidal neurons. The gradual enlargement was strongly dependent on protein synthesis and brain-derived neurotrophic factor (BDNF) action, often associated with spine twitching, and was induced specifically at the spines that were immediately enlarged by the synaptic stimulation. Thus, this spike-timing protocol is an efficient trigger for BDNF secretion and induces protein synthesis–dependent long-term enlargement at the level of single spines.

1 Laboratory of Structural Physiology, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033, Japan.
2 Center for NanoBio Integration, University of Tokyo, Tokyo 113-0033, Japan.
3 Department of Cell Physiology, National Institute for Physiological Sciences, and Graduate University of Advanced Studies (SOKENDAI), Myodaiji, Okazaki 444-8787, Japan.
4 PRESTO, Japan Science and Technology Agency, 4-1-8 Honcho, Kawaguchi, Saitama, Japan.
5 Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA 19102, USA.

* These authors contributed equally to this work.

{dagger} To whom correspondence should be addressed. E-mail: hkasai{at}m.u-tokyo.ac.jp

Read the Full Text


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Backpropagating Action Potentials Trigger Dendritic Release of BDNF during Spontaneous Network Activity.
N. Kuczewski, C. Porcher, N. Ferrand, H. Fiorentino, C. Pellegrino, R. Kolarow, V. Lessmann, I. Medina, and J.-L. Gaiarsa (2008)
J. Neurosci. 28, 7013-7023
   Abstract »    Full Text »    PDF »


ADVERTISEMENT
Click Me!

ADVERTISEMENT
Click Me!

To Advertise     Find Products

Science. ISSN 0036-8075 (print), 1095-9203 (online)